<b>Results:</b> Clinical trials found that miR-223-3p expressions were markedly different (more than 2-fold) between the acute KD group and the control group.
<b>Results:</b> In our microarray study, the mRNA levels of DNMT1 and DNMT3A were significantly lower while TET2 was higher in acute-stage KD patients compared to the healthy controls.
<b>Results:</b> We analyzed patients' DNA for the SNPs in B lymphoid tyrosine kinase, CD40, and coatomer protein complex beta-2 subunit, which had been associated with KD by literatures.
1,25-Dihydroxyvitamin D3 regulates T lymphocyte proliferation through activation of P53 and inhibition of ERK1/2 signaling pathway in children with Kawasaki disease.
1,25-Dihydroxyvitamin D3 regulates T lymphocyte proliferation through activation of P53 and inhibition of ERK1/2 signaling pathway in children with Kawasaki disease.
Kawasaki disease vasculitis may be triggered by aberrant activation of inflammatory cytokines mediated by IL-17 that is produced by Th17 cells that have been activated by some infectious agent(s).
KD significantly elevated beta-hydroxybutyrate levels, and there was no brain edema associated with rmTBI and KD therapy; behavioral assessment showed KD therapy significantly improved motor performance; magnetic resonance spectroscopy showed that rmTBI reduced the ratio of NAA/Cr and had no effect on the ratios of Cho/Cr and NAA/Cho whereas KD increased the ratio of NAA/Cr; double immunofluorescence staining showed KD therapy could significantly decrease microglial beclin-1 expression in the ipsilateral cortex.
CD40L expression on platelets from patients with KD was also significantly higher than in the FC group (8.20 +/- 0.41% vs 1.26 +/- 0.12%) and decreased after IVIG therapy. sCD40L levels were also significantly higher in KD patients with those of FC (9.69 +/- 0.45 ng/mL vs 2.25 +/- 0.19 ng/mL) but were not affected by IVIG treatment 3 days afterward (9.69 +/- 0.45 ng/mL vs 9.03 +/- 0.32 ng/mL).
ITPKC acts as a negative regulator of T-cell activation through the Ca2+/NFAT signaling pathway, and the C allele may contribute to immune hyper-reactivity in Kawasaki disease.
ITPKC acts as a negative regulator of T-cell activation through the Ca2+/NFAT signaling pathway, and the C allele may contribute to immune hyper-reactivity in Kawasaki disease.
ITPKC acts as a negative regulator of T-cell activation through the Ca2+/NFAT signaling pathway, and the C allele may contribute to immune hyper-reactivity in Kawasaki disease.
Tumor necrosis factor (TNF) and the TNF receptor superfamily (TNF-TNFR) plays very important roles in the pathogenesis of Kawasaki disease (KD) by leukocyte recruitment, upregulation of matrix-degrading enzymes and proinflammatory cytokines.
CD84, which facilitates immune responses and stabilizes platelet aggregates, is markedly up-regulated in KD CA in patients with acute and chronic arterial disease.
HLA-B*44 has been associated with KD in other smaller studies, and both HLA-C*15 and HLA-B*44 have biological mechanisms that could potentially be involved in KD pathogenesis.